After fully sequencing the latent HIV "provirus" genomes from 19 people being treated for HIV, scientists at Johns Hopkins Medicine report that even in patients who start treatment very early, the only widely available method to measure the reservoir of dormant HIV in patients is mostly counting defective viruses that won't cause harm, rather than those that can spring back into action and keep infections going.

Investigators from the National Institutes of Health have discovered that cells from HIV-infected people whose virus is suppressed with treatment harbor defective HIV DNA that can nevertheless be transcribed into a template for producing HIV-related proteins. This finding may affect scientists' understanding of the long-term effects of HIV infection and what a cure would require.

By watching brightly glowing HIV-infected immune cells move within mice, researchers at the Icahn School of Medicine at Mount Sinai have shown how infected immune cells latch onto an uninfected sister cell to directly transmit newly minted viral particles. These interactions allow HIV to spread efficiently between these immune cells, known as CD4+ helper T cells. The research, published online today in Cell Reports, challenges the long-held perception that the primary route of HIV infection of immune cells is from free-floating viral particles that move within tissue and blood fluids.

Viruses attack cells and commandeer their machinery in a complex and carefully orchestrated invasion. Scientists have longed probed this process for insights into biology and disease, but essential details still remain out of reach.

Acute HIV infection (AHI) contributes significantly to HIV transmission and may be important for intervention strategies seeking to reduce incidence and achieve a functional cure. In a study by the U.S. Military HIV Research Program (MHRP), Walter Reed Army Institute of Research, published in The New England Journal of Medicine, scientists enrolled and intensively followed a cohort of high-risk individuals, tracking their HIV status and characterizing the disease through the acute stages of HIV infection.

(image) This is Tariq Rana, Ph.D. Researchers at University of California, San Diego School of Medicine have discovered that HIV infection of human immune cells triggers a massive increase in methylation, a chemical modification, to both human and viral RNA, aiding replication of the virus. The study, published February 22, 2016 in Nature Microbiology, identifies a new mechanism for controlling HIV replication and its interaction with the host immune system.

New research findings published in the February 2016 issue of the Journal of Leukocyte Biology, suggest that a new therapeutic strategy for HIV may already be available by repurposing an existing prescription drug. The drug, an enzyme called adenosine deaminase, or ADA, ultimately may be able to activate the immune system against HIV and to help the immune system "remember" the virus to prevent or quickly eliminate future infection.

HIV drug resistance to tenofovir, an antiretroviral drug vital to most modern HIV treatment and prevention strategies, is surprisingly and worryingly common according to a large study led by UCL (University College London) and funded by the Wellcome Trust.

Antiretroviral therapies, or ART, have enabled people with HIV and AIDS to live much longer lives, transforming what was considered a death sentence into a chronic condition. Yet concerns for these patients remain. Up to half of people with HIV on these drug regimens have some sort of cognitive impairment, such as memory loss or problems with executive functioning, despite the virus being almost undetectable in their bodies.